Figure 1
From: TRPC3 positively regulates reactive oxygen species driving maladaptive cardiac remodeling
TRPC3 deletion suppresses TAC-induced LV dysfunction and dilation through Nox2 inhibition.
(a) Left ventricular end-diastolic pressure (LVEDP; left) and dP/dTmax (right) in TAC-operated TRPC3(+/+) (n = 13) and TRPC3(−/−) (n = 12) mice 6 week post-operation. (b) Myocardial malondialdehyde concentrations 1 week after TAC (n = 4). (c) Abundance of Nox2 protein in TRPC3(+/+) and TRPC3(−/−) hearts 1 week after TAC (n = 3). (d) Representative immunofluorescence images of TRPC3, p22phox, and caveolin-3 (Cav-3) in adult mouse cardiomyocytes isolated from muscle LIM protein-deficient hearts. (e) Representative immunofluorescence images of p22phox in adult mouse cardiomyocytes: green, anti-p22phox; blue, DAPI. (f) Relative abundances of p22phox and Nox2 mRNA in mouse hearts 1 week after TAC (n = 4). (g) Abundance of Nox2 protein in TRPC6(+/+) and TRPC6(−/−) hearts 1 week after TAC (n = 3). Error bars, s.e.m. *P < 0.05, **P < 0.01.
